As wild-type p53 reinforces the epithelial phenotype in a cell-autonomous manner, for example through the upregulation of miR-34 and miR-200 family members [113,114,115], it is intriguing to speculate that mutant p53 establishes a non-cell-autonomous tumor–stroma crosstalk, driven by exosomal miRNA secretion, that enhances TGF-β secretion by fibroblasts, to reinforce the pro-metastatic EMT phenotype of colorectal cancer cells. Here, TGFB1 is linked to colorectal cancer.